Jaceosidin inhibits NLRP3-mediated pyroptosis by activating SIRT1/NRF2 and ameliorating intestinal epithelial cell injury
Résumé
Purpose: To investigate the effect of Jaceosidin in ulcerative colitis (UC).Methods: An ulcerative colitis cell model was established by stimulating normal human colon mucosal epithelial cell lines (NCM460 cells) with lipopolysaccharide (LPS). The cells were treated with 5, 10, 20 or 40 μM Jaceosidin. Cell viability was performed using cell counting kit 8 (CCK8) assay. Oxidative stress was measured with superoxide dismutase (SOD), lipid peroxidation MDA, reduced glutathione (GSH), oxidized glutathione (GSSG), and human myeloperoxidase enzyme-linked immunoassay (ELISA) kits. The mRNA levels were determined by quantitative polymerase chain reaction (qPCR) assay, while protein levels of SIRT1, NRF2, NLRP3, caspase-1, TNF-α, IL-1β, and IL-6 were determined by western blotting.Results: Jaceosidin significantly inhibited oxidative stress and accumulation of inflammatory cytokines in LPS-induced NCM460 cells, as well as NLRP3-mediated cell pyroptosis (p < 0.05). Jaceosidin also inhibited activation of NLRP3 inflammasome by activating SIRT1/NRF2 pathway, thereby preventing NCM460 cell pyroptosis.Conclusion: Jaceosidin inhibits NLRP3-mediated pyroptosis, thus suggesting that jaceosidin is a potential lead for UC secondary to NLRP3 inflammasome.
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